PRDX2 plays an oncogenic role in esophageal squamous cell carcinoma via Wnt/β-catenin and AKT pathways

• A. L. Feng ^[2] ; X. Han ^[1] ; X. Meng ^[2] ; Z. Chen ^[2] ; Q. Li ^[2] ; W. Shu ^[2] ; H. Dai ^[2] ; J. Zhu ^[3]
  1. [1] Guangxi Medical University

     Guangxi Medical University

     China

     
  2. [2] Department of Oncology, Shandong Provincial Hospital Affiliated To Shandong University, 324# Jing 5 Road, Jinan, 250021, People’s Republic of China
  3. [3] Department of General Surgery, The First Affiliated Hospital of Shandong First Medical University, 16766# Jingshi Road, Jinan, 250014, People’s Republic of China

  Mostrar afiliaciones +
• Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 22, Nº. 10, 2020, págs. 1838-1848
• Idioma: inglés
• Texto completo no disponible (Saber más ...)
• Resumen

  • Purpose To investigate the role of PRDX2 in esophageal carcinoma (ESCA).

    Methods The expression of PRDX2 was detected in ESCA tissues. And PRDX2 expression in two ESCA cell lines was knocked down. Cell proliferation, metastasis and invasion were detected in these cells.

    Results Here, we found that PRDX2 expression was significantly increased in ESCA tissues and was associated with a poor prognosis in ESCA patients. In addition, PRDX2 expression was significantly associated with pathological grading, infiltration degree and 5-year survival time in ESCA patients. Next, we knocked down PRDX2 expression by PRDX2-shRNA transfection in two ESCA cell lines, Eca-109 and TE-1. Proliferation analysis indicated that in vitro PRDX2 knockdown decreased growth and clone formation of ESCA cells. Scratch and transwell assays indicated that cell migration and invasion were significantly inhibited by PRDX2 knockdown. In addition, PRDX2 knockdown inhibited cell cycle of ESCA cells and down-regulated Cyclin D1-CDK4/6. Moreover, PRDX2 knockdown regulated proteins involved in mitochondrial-dependent apoptosis, including increased Bax and Caspase9/3 and decreased Bcl2. Mechanism investigation indicated that PRDX2 knockdown led to inactivation of Wnt/β-catenin and AKT pathways.

    Conclusions Our data suggest that PRDX2 may function as an oncogene in the development of ESCA via regulating Wnt/β-catenin and AKT pathways. Our study fills a gap in the understanding of the role of PRDX2 in ESCA and provides a potential target for ESCA treatment.